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Indomethacin Inhibits Duodenal Mucosal Bicarbonate Secretion and Endogenous Prostaglandin E2 Output in Human Subjects

JOHN A. SELLING, M.D.; DANIEL L. HOGAN, B.A.; ANDREAS ALY, M.D., Ph.D.; MICHAEL A. KOSS, B.S.; and JON I. ISENBERG, M.D.
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Grant support: in part by grants AM 33491-02 and AM 07202 from the National Institutes of Health.

Presented in part at a Research Forum of the 86th Meeting of the American Gastroenterological Association in New York on 20 May 1985, and published in abstract form in Gastroenterology, 1985; 88:1580; and Acta Physiol Scand, 1985;124(suppl 542):357.

▸Requests for reprints should be addressed to Jon I. Isenberg, M.D.; Division of Gastroenterology, UCSD Medical Center (H-811-D), 225 Dickinson Street; San Diego, CA 92103.


San Diego, California; and Stockholm, Sweden


© 1987 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1987;106(3):368-371. doi:10.7326/0003-4819-106-3-368
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Nonsteroidal anti-inflammatory drugs are a frequent cause of gastric and duodenal mucosal injury. We examined the effect of indomethacin on duodenal mucosal bicarbonate secretion and prostaglandin output in healthy subjects. Subjects received either 50 mg of indomethacin or placebo orally 13 hours and 1 hour before study. A 4-cm segment of proximal (the duodenal bulb) or distal (10 to 14 cm beyond the pylorus) duodenum was isolated and perfused with 154 mM NaCI containing a nonabsorbable marker. In the proximal duodenum indomethacin reduced both basal and acid-stimulated bicarbonate secretion by approximately 65% (p < 0.01); in the distal duodenum indomethacin decreased basal and acid-stimulated bicarbonate output by approximately 45% (p < 0.01). Oral indomethacin inhibited basal and acid-stimulated duodenal prostaglandin E2 output in both the proximal and distal duodenum. We conclude that, by decreasing duodenal mucosal bicarbonate production and prostaglandin output in humans, oral indomethacin, in two doses of 50 mg each, impairs an important duodenal defense mechanism.

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